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短链脂肪酸通过抑制基因素脱乙酶来刺激树突细胞中的树突延长
Takuho Inamoto1, Kazuyuki Furuta1, Cheng Han1
1Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, Japan.
The FEBS journal
|August 30, 2023
概括
短链脂肪酸 (SCFA) 通过抑制基因组脱乙酶 (HDAC) 和激活信号通路来促进树突细胞树突延长. 这增强了抗原的吸收和呈现,这对免疫反应至关重要.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 树突细胞是通过树突细胞呈现抗原的关键免疫细胞.
- 短链脂肪酸 (SCFA) 调节免疫反应,但它们对树突细胞树突的作用尚不清楚.
研究的目的:
- 为了研究SCFA对树突细胞树突延长的影响.
- 阐明潜在的分子机制和功能后果.
主要方法:
- 利用树突细胞系 (DC2.4) 和初级小鼠骨髓衍生的树突细胞.
- 评估了树突延长,信号通路激活 (SFK,PI3K,Rho GTPases),动因聚合和抗原吸收.
- 采用了组织素脱乙酶 (HDAC) 抑制剂和SCFA受体激动剂.
主要成果:
- 在树突细胞中,SCFA显著诱导了树突延长.
- 这种效应是由Src家族激酶 (SFK) /酸丁醇-3激酶 (PI3K) /Rho家族GTPase通路和actin聚合介导的,而不是SCFA受体.
- 抑制HDAC也促进了延长,这取决于SFK/PI3K/Rho通路.
- 酸治疗增强了抗原吸收和MHCII类介导的抗原呈现.
结论:
- 通过HDAC抑制和SFK/PI3K/Rho通路的激活,SCFA促进树突细胞树突延长,从而导致增强的动氨酸聚合.
- 这一过程改善了树突细胞在抗原吸收和呈现方面的功能,可能会增强适应性免疫力.
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